搜索结果：Diseases (Basel, Switzerland)

This study explores Serbia's rich ethnopharmacological heritage by systematically documenting the traditional use of medicinal plants for treating skin diseases during the 19th and 20th centuries. Drawing on key ethnographic sources-including monographs, scholarly articles, and field reports-the review analyzes historical records of folk medicine practices and their cultural contexts. A total of 164 plant species from 63 botanical families, as well as one mushroom species, were identified as being used in the treatment of skin-related conditions classified according to the International Classification of Primary Care. Reported ailments were grouped into three main categories: hair and scalp disorders, bites, and various inflammatory skin conditions such as eczema and psoriasis. Remedies for wound healing were the most frequently documented, both in terms of application and diversity of plant species employed. By preserving and systematizing this historical knowledge, the study provides a valuable foundation for future pharmacological and dermatological research, highlighting the continued relevance of traditional remedies in modern clinical practice.

Background/Objectives: Therapeutic drug monitoring (TDM) of immunosuppressants is essential in treating pediatric kidney diseases; however, repeated venipuncture is burdensome in children. We evaluated whether minimally invasive fingerstick capillary sampling combined with liquid chromatography-tandem mass spectrometry (LC-MS/MS) provides results analytically comparable to those of conventional venous sampling. Methods: Capillary whole blood (2.8 µL) was collected via fingersticks from pediatric patients receiving mycophenolate mofetil, with or without tacrolimus (TAC) or cyclosporine A (CsA). Drug concentrations were quantified using a previously validated simultaneous LC-MS/MS method and compared with conventional venous sampling using linear regression and Bland-Altman analyses. Results: Seventy-four paired samples from 21 patients were analyzed. Strong correlations were observed between capillary and venous samples for mycophenolic acid (MPA), TAC, and CsA (R2 > 0.90). Hematocrit correction improved agreement for MPA. Bland-Altman analyses demonstrated acceptable bias across analytes. Conclusions: Fingerstick-based microvolume sampling combined with LC-MS/MS provides analytically reliable immunosuppressant quantification in pediatric patients. Although larger clinical validation is required, this minimally invasive approach may reduce procedural burden and may support future outpatient or home-based TDM strategies.

Background/Objectives: Inherited retinal diseases (IRDs) represent a genetically heterogeneous group of disorders caused by mutations in over 280 genes with more than 3100 identified variants. While gene-specific replacement therapies have achieved landmark success with voretigene neparvovec (Luxturna) for biallelic RPE65-associated retinal dystrophy, developing individual therapies for each genetic subtype remains impractical. This review examines gene-agnostic therapeutic approaches utilizing neuroprotection and immunomodulation that target common pathophysiological mechanisms shared across multiple IRD genotypes. Methods: We reviewed the literature on neuroprotective and immunomodulatory gene therapy strategies for IRDs, focusing on neurotrophic factors and complement system modulation. Results: Neuroprotective approaches delivering neurotrophic factors-including pigment epithelium-derived factor (PEDF), ciliary neurotrophic factor (CNTF), rod-derived cone viability factor (RdCVF), brain-derived neurotrophic factor (BDNF), fibroblast growth factors (FGFs), glial cell line-derived neurotrophic factor (GDNF), and proinsulin-have demonstrated photoreceptor preservation across multiple preclinical IRD models regardless of the underlying genetic mutation. The recent FDA approval of CNTF cell-based gene therapy (Encelto) for macular telangiectasia type 2 validates this therapeutic paradigm. Complement system inhibition represents another gene-agnostic strategy, with intravitreal complement inhibitors approved for geographic atrophy secondary to age-related macular degeneration and gene therapy approaches targeting C3, C5, or delivering soluble complement regulators under investigation for IRDs. Combination strategies simultaneously addressing multiple pathogenic pathways may offer synergistic benefits. Conclusions: Gene-agnostic approaches targeting neuroprotection and immunomodulation offer a therapeutic paradigm capable of benefiting patients across the spectrum of IRD genotypes, potentially transforming treatment for conditions where mutation-specific therapies remain unavailable.

Inflammatory processes drive a heterogeneous spectrum of diseases, including cardiovascular (CV), neurodegenerative, autoimmune, rare, and viral disorders, which together account for a major global disease burden. Despite diverse clinical manifestations, these conditions share systemic endothelial dysfunction (ED) as a common pathophysiological hallmark. The retina, accessible through non-invasive imaging, provides a unique window into systemic microvascular health. Over the past decades, retinal vessel analysis (RVA), both static and dynamic, has emerged as a robust tool for detecting and predicting microvascular alterations in inflammatory diseases. Large population-based cohorts, including the Atherosclerosis Risk in Communities (ARIC, n>9,000 participants) study and the Rotterdam Study (n>5,000), have shown that retinal diameter changes independently predict incident CV events and all-cause mortality. Recent UK Biobank (n>45,000) analyses further demonstrate incremental value in stroke prediction beyond traditional risk factors (AUC 0.739 to 0.752; p<0.001). Other retinal imaging modalities, such as optical coherence tomography angiography (OCTA) and adaptive optics (AO), provide complementary high-resolution structural data on capillary architecture and perfusion integrity. The retinal vascular phenotype reflects both shared and disease-specific mechanisms of ED. Therefore, accurate interpretation of retinal biomarkers requires an understanding of the molecular pathways that shape ED across disease entities, thereby forming the conceptual foundation of oculomics. We synthesize current evidence linking systemic ED to retinal microvascular structure and function across major categories of inflammatory disease. We integrate findings from static and dynamic RVA, OCTA, and AO, discuss their mechanistic interpretation within the emerging framework of oculomics, and critically evaluate challenges for clinical translation. Finally, we outline how artificial intelligence (AI) may facilitate robust, scalable implementation of retinal biomarkers for risk stratification, disease monitoring, and outcome prediction. This review moves beyond modality-specific descriptions to propose a unified biological and translational framework for retinal biomarkers.

In major wheat-growing regions, rust diseases and common bunt significantly reduce wheat productivity, especially in years with favorable conditions for phytopathogen development and limited resistant cultivar use. Thus, the development of genetically resistant wheat cultivars carrying combinations of valuable resistance genes is an effective strategy to mitigate these losses. In this study, 156 advanced winter wheat breeding lines were evaluated for resistance to yellow (stripe) rust, leaf (brown) rust, and common bunt under an artificial infection background. Concurrently, molecular screening was performed using DNA markers to detect rust (Yr5, Yr10, Yr15, Lr9, Lr34/Yr18, and Lr37/Yr17) and common bunt resistance genes (Bt8, Bt9, Bt10, Bt11, and Bt12). Based on the integrated analysis of phenotypic and DNA marker-based molecular data, fourteen and five lines resistant to common bunt and yellow rust, respectively, were identified, and alleles associated with resistance were also detected. Notably, one line (9909) exhibited high resistance to both rust diseases and common bunt. These selected advanced breeding lines represent promising candidates for the development of wheat cultivars with enhanced disease resistance, thereby supporting sustainable productivity in wheat-growing regions.

Two-pore domain potassium (K2P) channels are the most recently identified family of potassium channels. They are regarded as the largest group of background "leak" channels, encoded by 15 mammalian KCNK genes, and divided into six subfamilies (TWIK, TREK, TASK, TALK, THIK, and TRESK). These channels have a role in stabilizing the resting membrane potential. Their widespread presence in the heart and vasculature supports cellular homeostasis by regulating cardiac rhythm, vascular tone, and protection against ischemic stress. The TASK, TWIK, and TREK subfamilies are the most abundantly expressed K2P channel subfamilies in the cardiovascular system, and dysregulation of specific members has been strongly linked to the development of major cardiovascular diseases. Mutations in TASK-1 have been identified in patients with pulmonary arterial hypertension, providing human genetic evidence linking K2P dysfunction to pulmonary vascular disease. While alterations in other K2P channels, such as TREK-1, have been demonstrated in preclinical studies where reduced channel activity is associated with ischemia-reperfusion injury and promotes cardiac arrhythmias. Growing evidence suggests that K2P channels could serve as promising therapeutic targets, with pharmacological activation of TASK-1 and TREK-1, for instance, that might help restore vascular tone, reduce remodeling, and offer cardioprotection. Their unique leak-channel properties enable the development of highly selective treatments. This review addresses the molecular biology, physiological roles, and disease relevance of K2P channels in the cardiovascular and pulmonary systems, emphasizing their potential as targets for innovative therapies in cardiovascular diseases.

Helichrysum odoratissimum (L.) Less. is used as a traditional medicine in South Africa to treat tuberculosis, abdominal pains, heartburn, coughs, colds, female sterility, eczema and wounds. In Uganda, the leaves are used to treat dental/oral diseases. This review aims to provide detailed information on the traditional uses, essential oils, phytochemistry, in silico studies, and pharmacological studies and propose possible future research directions on this widely investigated species. The data was gathered from various online electronic databases such as Science Direct, Scopus, Google Scholar, Web of Science, SciFinder, Wiley Online, SpringerLink, and PubMed. Reports on the essential oil composition of H. odoratissimum showed the dominance of monoterpenoids and sesquiterpenoid compounds. Several studies also reported the isolation of the non-volatile compounds, which were mainly flavonoids and terpenes. The species has been reported to have pharmacological activities such as antimicrobial, antimycobacterial, antioxidant activity, antidiabetic, antiproliferative, anti-inflammatory activity and antityrosinase activity. The most important study on H. odoratissimum was a clinical trial in human participants in South Africa addressing its in vivo irritancy potential. However, further research on the clinical and scientific aspects is needed to justify some of its other medicinal uses.

Neuroinflammation is determinant in the progression of neurodegenerative diseases. One of the main mechanisms underlying this process involves the persistent activation of glial cells. Persistent activation of glial cells induces proinflammatory transcription factors and the release of cytokines, chemokines, and reactive oxygen species that exacerbate cellular dysfunction. This neurotoxic environment promotes neuronal death, while the products of cellular damage feed back into glial activation, establishing a self-sustaining pathogenic cycle that drives neurodegeneration. Alkaloids present in Amaryllidaceae plants support the use of this resource in folk medicine, displaying potent effects as acetylcholinesterase inhibitors and allosteric modulators of nicotinic receptors (nAChR). In this study, a murine microglial cell (IMG) model of LPS-induced inflammation was used to evaluate the involvement of &#x3b1;7 and &#x3b1;4&#x3b2;2 nAChRs in glioprotection and neuroprotection of SH-SY5Y cells against 6-hydroxydopamine (OHDA). GC-MS analysis revealed differences in the alkaloid profile between in vitro cultures with fructose and wild-type Rhodophiala pratensis. Homolycorine-type, norbelladine-type and crinine-type alkaloids produced in vitro reduced LPS-induced inflammation (5 &#xb5;g/mL), possibly via &#x3b1;7 and &#x3b1;4&#x3b2;2 nAChRs, and showed a protective effect against OHDA-induced oxidative stress (1-3 &#xb5;g/mL) and inhibited AChE and BuChE (24-78 &#xb5;g/mL).

Background/Objectives: Mango bacterial angular leaf spot, caused by Xanthomonas citri pv. mangiferaeindicae (Xcm), is one of the most destructive bacterial diseases of mango, resulting in significant economic losses to the mango industry. Copper-based bactericides have been widely used for decades to control this disease, leading to increased copper resistance in the pathogen and heightened environmental risks. However, the copper resistance mechanisms of Xcm remain incompletely understood. Methods: In this study, we used Xcm GXBS06 isolated from major mango cultivars in Guangxi, China. We analyzed the homologs of known copper resistance-related genes in Xcm and found that these genes are relatively conserved across different strains. The functions of six important known copper resistance gene homologs in Xcm were investigated. Among them, five were functionally characterized by gene deletion, while the remaining one was characterized by overexpression because deletion was unsuccessful. Results: The result showed that copB is a critical copper resistance-related gene in Xcm. However, its deletion neither affects H2O2 tolerance nor virulence determinants such as extracellular polysaccharide production, biofilm formation, or cell motility. Additionally, it did not impact pathogenicity or bacterial growth within the host. The expression of copB was significantly induced at copper sulfate concentrations of 0.2 mM and 0.6 mM. Conclusions: These findings contribute to a better understanding of the copper resistance mechanisms in Xcm and provide a foundation for further studies on the biological control of this pathogen.

Tick-borne diseases (TBDs) represent an increasing public health threat globally. Climate change has facilitated tick range expansion and extended active seasons, contributing to rising TBD incidence rates. In Switzerland, TBDs represent a major health concern. This study aims to characterise patterns in spatio-temporal distribution of tick-borne pathogens (TBPs) in ticks removed from humans across Switzerland, examine associations between tick developmental stages and TBP infection prevalence, and analyse co-infection patterns amongst different TBPs. We employed the "Tick Prevention" citizen science app to collect spatial and temporal data on tick bite incidents and to obtain tick specimens for pathogen screening throughout Switzerland during 2018-2020. Specimens underwent DNA extraction for TBP detection. Quantitative PCR targeted different TBPs at genus and species levels. Data analysis examined TBP infection prevalence in submitted ticks across geographic regions, seasons, and tick developmental stages, including co-infection patterns in ticks. Of 1056 tick specimens, 352 (33.3%) tested positive for at least one TBP, with Borrelia spp. (16.3%) and Rickettsia spp. (12.69%) showing higher infection prevalence than other TBPs, including Neoehrlichia mikurensis (5%), Anaplasma phagocytophilum (1.8%), Chlamydiales (1.8%), and Babesia spp. (1.7%). Co-infections occurred in 59 specimens (5.6%), predominantly dual infections (5.2%), with Borrelia spp. and N. mikurensis representing the most common co-infection pattern. Among 58 larvae, 898 nymphs, and 96 adult ticks examined, tick infection prevalence increased with developmental stage, rising from larvae (18.9%) to nymphs (32.6%) to adults (48.9%), consistent with pathogen acquisition through successive blood meals during tick development. Spatially, TBPs were detected across 70 of 76 Swiss administrative regions, with most TBPs displaying uniform distribution. Temporally, tick-human encounters peaked during May-June (59.7% of announced events), with TBP detection rates remaining steady (28-37%) across the tick-active months from April to September. One-third of examined ticks harboured at least one TBP, with weighted models indicating infection prevalence in submitted ticks could reach 45% in certain Swiss Plateau regions. These findings emphasise the importance of continued tick and TBP surveillance programmes to inform public health interventions and prevention.

The objective of this study was to evaluate the effects of potassium (K) on disease severity and the chemical composition of Megathyrsus maximus cultivars. The experiment was conducted in a randomized block design in a 6 &#xd7; 4 factorial arrangement, consisting of six Megathyrsus maximus cultivars (Massai, Momba&#xe7;a, Tamani, Tanz&#xe2;nia, Qu&#xea;nia, and Zuri) and four K doses (0, 205, 410, and 820 mg dm-3). The severity of the leaf spot complex, caused by Bipolaris maydis and B. yamadae, was assessed using a diagrammatic scale. A significant interaction between K doses and cultivars was observed for all evaluated diseases. At K doses of 0 and 205 mg dm-3, the Tanz&#xe2;nia cultivar showed lower leaf spot severity compared with the other cultivars, whereas at higher doses, no disease symptoms were observed in any cultivar. The area under the disease progress curve (AUDPC) for mosaic followed a linear model only for the Tanz&#xe2;nia cultivar, whereas quadratic regression models best described the response for the remaining cultivars, with maximum mosaic severity values of 67.74% for Qu&#xea;nia, 72.34% for Momba&#xe7;a, 76.99% for Zuri, 74.88% for Massai, and 68.93% for Tamani. Increasing K doses reduced the severity of both the leaf spot complex and mosaic. However, the leaf spot complex did not affect the nutritional value of the evaluated cultivars.

Background: Respiratory syncytial virus (RSV) is a leading global pathogen of acute lower respiratory tract infection, posing significant risks to infants, the elderly, and immunocompromised patients. Artemisia argyi Levl.et Vant Extract (AALE) and its active components have a variety of pharmacological effects, but their anti-RSV potential remains unclear. The aim of this study is to investigate the anti-RSV activity of AALE and parthenolide and its underlying mechanisms. Methods: Cell counting kit-8 (CCK-8) assay was used to determine the anti-RSV activities of AALE and parthenolide. Time-of-addition assay and phase of action analysis were used to explore the effect of drugs on the viral replication cycle. Quantitative polymerase chain reaction (qRCR), immunofluorescence (IF) and Western blot (WB) were used to investigate the effects of AALE and parthenolide on RSV-F gene and protein and on RIG-I/TLR-3 pathway related molecules in vitro. In vivo antiviral efficacy was verified by hematoxylin-eosin (HE) staining for lung histopathology, quantitative real-time PCR (qPCR) quantification of RSV-F, RIG-I, TLR-3, IRF3, IL-6, and IFN-&#x3b2; gene expression in lung tissues, and enzyme-linked immunosorbent assay (ELISA) for serum IL-6 and IFN-&#x3b2; levels. Results: AALE exhibited the strongest anti-RSV activity among the extracts (SI = 27.6), while parthenolide was the most potent monomeric compound (SI = 8.19). In vitro, both AALE and parthenolide were effective in the co-treatment and post-treatment models, reducing RSV-F gene and F protein levels in infected cells. Furthermore, they alleviated RSV infection by regulating RIG-I and TLR-3 pathway-related genes and proteins. In vivo, AALE and parthenolide suppressed lung index and RSV proliferation, attenuated lung injury, and down-regulated RIG-I, TLR-3, IRF3, IL-6, and IFN-&#x3b2; expression in the lungs of RSV-infected mice. Conclusions: AALE and its component parthenolide can inhibit the invasion and replication of RSV, making it a potential candidate for the treatment of RSV-related diseases.

Management of patients with refractory or frequently relapsing (r/r) immune thrombotic thrombocytopenic purpura (iTTP) remains challenging, with no established consensus on optimal therapeutic strategies. In recent years, plasma-cell depletion with daratumumab, a monoclonal antibody against CD38, has been used successfully for treatment-resistant patients with various autoimmune diseases, including iTTP, although long-term data remain limited. To assess the efficacy, durability, and safety of daratumumab in patients with r/r iTTP. We retrospectively analyzed 8 daratumumab treatment episodes in 5 patients with r/r iTTP, treated at 3 Swiss tertiary centers, with a median follow-up after daratumumab of 44 months (range, 34-65 months). Serial a disintegrin and metalloproteinase with thrombospondin type 1 motif 13 (ADAMTS-13) activity and inhibitor levels, clinical outcomes, and adverse events were assessed. Daratumumab induced rapid and robust ADAMTS-13 recovery in 7 of 8 episodes. All responding patients achieved complete ADAMTS-13 remission within 1 and 3 weeks. Mean ADAMTS-13 relapse-free survival following daratumumab was 32 months, with 7 of 8 episodes remained in complete ADAMTS-13 remission at 12 months. Nonetheless, ADAMTS-13 relapse occurred in 4 of 5 patients during long-term follow-up. Two patients experienced mild to moderate infusion-related adverse reactions. Our findings support daratumumab as an effective and well-tolerated therapeutic option for patients with r/r iTTP, particularly those unresponsive to rituximab and other immunosuppressants.

The leishmaniases are a group of neglected tropical diseases caused by kinetoplastid protozoa of the genus Leishmania, transmitted by phlebotomine sandflies. In the absence of a human vaccine, current chemotherapeutic options remain suboptimal due to limited target selectivity, high cost, restricted availability in endemic low-resource regions, and escalating parasite resistance. This review highlights recent advances in rational drug design directed at the kinetoplast-a distinctive mitochondrial organelle critical for parasite viability. Different targets (e.g., kDNA, G-quadruplex, topoisomerases) and innovative approaches employing mitochondrion-targeted small molecules are discussed, as well as ligand-functionalized nanoparticle delivery systems that can transport bioactive agents to the parasite's mitochondrial microenvironment. These strategies highlight the kinetoplast's strong translational relevance as a selective antileishmanial target. By exploiting its unique molecular machinery, these strategies may offer improved parasite selectivity, although potential mitochondrial liabilities in host cells must be carefully evaluated.

In recent years, yeast glucan particles (YGPs) have garnered significant attention as novel oral drug delivery carriers, owing to their superior biocompatibility, specific targeting capabilities, and intrinsic immunomodulatory properties. The yeast cell wall is primarily composed of &#x3b2;-glucan and mannan, with minor amounts of proteins and lipids. Among these, &#x3b2;-1,3-glucan serves as the pivotal functional component. It not only provides a physical barrier protecting payloads from gastric acidity and enzymatic degradation but also functions as a targeting ligand. By specifically binding to M cells in Peyer's patches and Dectin-1 receptors on macrophages and dendritic cells, &#x3b2;-1,3-glucan facilitates precise drug delivery to gut-associated lymphoid tissue (GALT) or macrophage-rich inflammatory sites. Consequently, &#x3b2;-1,3-glucan-based YGPs demonstrate immense potential in oral targeted delivery systems for macrophage-associated pathologies. However, native YGPs, constrained by their inherent porous architecture and relatively simple physicochemical properties, often fall short of meeting the complex requirements for precise encapsulation, controlled release, and multifunctionality. To address these limitations, current research is actively exploring the functionalization of YGPs with various composite materials to engineer advanced delivery platforms. This review introduces the composition, structural characteristics, and fabrication methodologies of YGPs, alongside their specific merits and limitations in oral drug delivery. Furthermore, it critically analyzes strategies for modifying YGPs with composite materials to overcome delivery barriers. Finally, the review discusses their therapeutic applications across various diseases and outlines future developmental trends.

Neuropsychiatric and neurodegenerative disorders impose a substantial global health burden, yet progress in mechanism-based therapy remains limited by clinical heterogeneity and an incomplete understanding of disease biology. Emerging evidence implicates ferroptosis-an iron-dependent form of lipid peroxidation-driven cell death-as a shared pathogenic process across primary psychiatric disorders and neurodegenerative diseases with prominent neuropsychiatric features. In this review, we synthesize evidence from major depressive disorder, schizophrenia, substance use disorders, Alzheimer's disease (AD), and Parkinson's disease (PD), highlighting ferroptosis as a common mechanism linking iron dyshomeostasis to neuronal dysfunction. Mechanistically, ferroptosis is organized around three interconnected modules: amino acid metabolism, lipid peroxidation, and iron handling. These pathways converge on mitochondrial dysfunction, oxidative damage, and neuroinflammatory amplification. We further propose that each disorder displays a distinct ferroptosis signature, including dopamine quinone-mediated GPX4 loss in PD, AICD-dependent transcriptional reprogramming in AD, and inflammatory-glutamatergic lowering of the ferroptotic threshold in depression and schizophrenia. Together, these insights position ferroptosis as a candidate framework for biomarker development, patient stratification, and mechanism-informed therapeutic intervention across neuropsychiatric disease.

The human genome produces a large repertoire of non-coding RNAs (ncRNAs) with important regulatory roles in development, physiology, and most of diseases. Among these, long non-coding RNAs (lncRNAs) have emerged as key modulators of gene expression, chromatin organization, and cellular homeostasis, despite displaying remarkably low primary-sequence conservation across species. This apparent evolutionary paradox questions the limitations of predicting biological function based on conservation, particularly across different biological domains. Here, we examine current evidence on lncRNA evolution, with a focus on their roles in metabolic regulation compared with neurobiological processes. We hypothesize that lncRNAs involved in ancient and conserved pathways such as metabolism may be under stronger evolutionary constraint than those associated with higher-order, species-specific traits, although available data support a more nuanced interpretation. Functional importance often correlates poorly with linear sequence conservation and instead appears to depend on higher-level features, including RNA secondary or tertiary structure, genomic context, regulatory architecture, and interactions with conserved molecular partners. We propose a systematic comparative framework to empirically assess conservation among metabolism- and neuro-associated lncRNAs using phylogenetic, syntenic, structural, and expression-based metrics. Finally, we discuss the therapeutic implications of lncRNA biology, highlighting how a deeper understanding of their evolutionary and mechanistic properties may inform the development of more precise and effective RNA-targeting strategies. Together, these insights underscore the non-coding transcriptome as a critical frontier for both fundamental biology and precision medicine.

Background/Objectives: Thymic stromal lymphopoietin (TSLP) is central to the pathogenesis of atopic dermatitis (AD) and a promising therapeutic target. However, developing small-molecule TSLP inhibitors is challenging due to the difficulty in disrupting the TSLP-TSLPR interface. This study aimed to explore naturally sourced blockers of the TSLP-TSLPR interaction and identify novel candidate compounds for AD treatment. Methods: HuT78 cells were stimulated with PMA, ionomycin, and TSLP to establish an AD model. Inflammatory cytokines were measured by qRT-PCR and ELISA. JAK/STAT signaling was analyzed by Western blot. In female BALB/c mice, DNCB-induced AD-like skin lesions were topically treated with test compounds, followed by histopathological and immunohistochemical assessment. Results: Eight compounds were screened, and their key structural features were elucidated via structure-activity relationship (SAR) analysis. Among them, kaempferol-7-O-glucoside (K-7-G) emerged as the most potent candidate. It interfered with the TSLP-TSLPR interaction, selectively inhibited TSLP-mediated JAK2/STAT5 phosphorylation, and significantly downregulated IL-4 (p < 0.0001) and IL-13 (p < 0.001) levels. Topical application of 1% K-7-G significantly alleviated AD-like symptoms in a mouse model, decreasing dorsal skin thickness, dermatitis score, and scratching frequency while restoring the expression of filaggrin, loricrin, and occludin (p < 0.0001). Meanwhile, it significantly reduced key inflammatory mediators in a concentration-dependent manner, including TSLP, IL-4, IL-13, TNF-&#x3b1;, IFN-&#x3b3;, and IgE. Conclusions: This study demonstrates that K-7-G is a novel natural TSLP inhibitor capable of blocking the TSLP-TSLPR signaling pathway and effectively improving AD symptoms. Further research may explore its therapeutic potential in other inflammatory diseases.

Medicinal plants have a long history of usage in the treatment and management of human and animal diseases and ailments [...].